Unit 2 - Bacterial Infections of the Mouth and Pharynx Flashcards
what are viral causes of pharyngitis?
Epstein-Barr virus
Adenoviruses
Herpes simplex virus type 1
Coxackie virus
what are fungal causes of pharyngitis?
Candida albicans
what are bacterial causes of pharnygitis?
Streptococcus pyogenes
Corynebacterium diphtheriae
Neisseria gonorrhoeae
what does pharyngitis examination typically reveal?
- inflammation of pharynx, tonsils, uvula, with exudate
- cervical lymphadenopathy
- fever
what percentage of pharyngitis are caused by group A streptococci? which one specifically?
30% Streptococcus pyogenes
bacteriology of group A streptococci?
beta-hemolytic (complete clear hemolysis)
- G+ (like all streptococci)
- bacitracin sensitive
- cocci grow in chains
- react with Lancefield group A antiserum
what are virulence factors of group A streptococci? what do they cause?
- pili (attachment)
- streptokinase (tissue lysis)
- streptodornase (digests DNA)
- hyaluronidase (digests CT)
- pyrogenic toxin (fever, super Ag, toxic shock)
- erythrogenic toxin (skin rash)
how does one diagnose pharyngitis from group A streptococci?
suggested by family or social history
- rapid Ag detection assays can identify, but prone to false negative results
- swab, culture, bacitracin sensitive, and G+ is accurate but slow
- NOT direct examination of smear, as can look identical to other things
what is the reservoir from group A streptococci? transmission?
Streptococcus pyogenes is carried in pharynx and skin
- carriers not symptomatic, but can still infect others
- transmit via contact or saliva
what are hemolysins in relation to group A strep? which one is diagnostically useful?
not virulence factors, but can identify streptococci b/c produce hemolysis on blood agar plates
- streptolysin O is highly antigenic, inducing short-lived IgM Ab which is diagnostically useful
- other toxins explain pathogenesis of infections
what are group A strep sensitive to?
penicillin, erythromycin, cephalosporins, and bacitracin
what are complications of streptococcal pharyngitis?
- tonsillitis
- middle ear infections
- mastoiditis
- meningitis
- scarlet fever
- rheumatic fever
*generally from orpharynx
explain types of tonsillitis from group A strep
- peritonsillar abscess (may need inscision to get pus out)
- Ludwig’s angina (spreads under tongue and swells such that it’s hard to breathe due to asphyxia)
what happens in ear infections from group A strep?
occurs in middle ear (also caused by S. pneumoniae or H. influenxa)
- may be permanent if eustacian tube closes off
- may be able to spread up to mastoids (mastoiditis)
- treat with Grommet tube to drain middle ear
how does mastoiditis from group A strep come about?
if recurrent middle ear infections occur
-can swell behind ear such that one sticks out
explain meningitis due to group A strep?
occurs if bacteria spread from middle ear infection or mastoiditis
-also caused by N. meningitides and S. pneumoniae
explain scarlet fever due to group A strep?
due to exotoxin encoded by bacteriophage that carries gene for erythrogenic toxin
- skin and tongue rash (strawberry tongue)
- they go away when the sore throat is gone, and not effectively treated by cream
explain rheumatic fever etiology due to group A strep?
most serious complication of sore throats
- post-streptococcal condition that arises around 3 weeks after resolution of group A (M3/5/13 strains)
- autoimmune condition with fever, polyarthritis, and inflammation of heart leading to permanent deformation (endocarditis; lesions are sterile)
- children 6-15 are at risk
- recurrences are common, and patients may need future prophylactic Ab for dentistry and minor surgical procedures
what can prevent group A strep infection?
no vaccines, despite many potent Ag
- prophylactic Ab fro patients who had post-streptococcal diseases
- treatment of carriers not recommended
- tonsillectomy reduces risk of future infections in some studies
how do you treat group A strep?
not essential, as the infection is self-limiting
- antibiotics can shorten symptoms by 16 hours and reduce complications
- systemic penicillin G, amoxicillin, erythromycin, or cephalosporins are suitable
- drug resistance is not a serious problem
- patients with a history of rheumatic fever need special attention
what are clinical features of rheumatic fever from group a strep?
- fever
- polyarthritis
- heart murmur (vasculitis, myocarditis, endarteritis, Aschoff body)
- Sydenham’s chorea (rare)
- duration can be several weeks or months
- case fatality rate is 2-5%
how is the diagnosis of rheumatic fever made?
clinical features plus presence of IgM anti-streptolysin O Ab
- heart lesions and inflammed joints are sterile
- there is no bacteremia
explain the pathogenesis of rheumatic fever?
autoimmune with certain M-proteins (M3/5) - although immune pathogenesis hasn’t been demonstrated directly
-certain HLA types are more common in patients than background population
rheumatic fever prevalence?
- prevalence has been reducing gradually over last 60+ years
- rheumatic fever once a compliccation of ~3% streptococcal sore throats, now 0.3%
- incidence is 50% in patients with a prior attack
how can rheumatic fever carditis resolve?
resolves with fibrosis of endocardium, or calicification, often with permanent valve distortion
-patients are at life-long risk of endocarditis, and may need antibiotics at times of likely bacteremia (dental extractions)
treatment of rheumatic fever?
anti-inflammatory drugs (aspirin, steroids)
- no antibacterial therapy is indicated
- later, replacement of heart valves may be necessary
prevention of rheumatic fever?
if have history of it, should use aggressive anti-bacterial therapy in the event of later streptococcal infections
explain bacteriology of Streptocccus viridans?
(includes S. sanguis and S. mutans)
-alpha-hemolytic (partial hemolysis), optochin-resistant, G+, catalase -
what are virulence factors of S. viridans?
sugar-metabolizing enzymes and extracellular polysaccharides
-turns LMW sugars to HMW sugars (dental plaque due to biofilms) or acids (demineralization)
how does one diagnose dental carries?
six-montly dental examinations show early demineralization
-lab testing not informative since bacteria are part of normal flora of mouth in 100% of people
what are complications of dental carries?
pupitis, abscesses, and cellulitis
-bacteremia and endocarditis may follow dental treatment of susceptible patients
how does one treat dental carries?
dental treatment to remove decalcified tissue
-acute abscesses can be treated temporarily with penicillin, erythromycin, or cephalosporins are of limited value, but dental extraction is more effective
what percent chance to people have of getting S. viridans bacteremia if the undergo…
- extraction of first 4 premolars
- single extraction
- polishing teeth
- palcing bands
- adjusting bands?
- 51%
- 38.5%
- 24.5%
- 10%
- 0%
explain the etiology of endocarditis?
previous rheumatic fever causes distortion of endothelium in heart, leading to turbulent blood flow
- sticky bacteria that come into contact with distorted endothelium can attach and replicate
- infection can be very persistent
- damage to heart may be continuous
- valves are particularly susceptible
explain treatment of endocarditis?
prolonged antibiotics
- replacement of heart valves carries risk of new valve becoming infected
- 50% of patients die despite treatment
what are heart vegetations foci of? what do antibiotics do?
infection and/or metastatic disease
- valves are gradually destroyed
- antibiotics don’t penetrate vegetation
what are causes of endocarditis?
- usually caused by S. viridans
- drug abusers or infected IV lines have S. aureus
- HACEK group of G- rods
how do you make a diagnosis of endocarditis?
variable clinical features, confirmed by cardiac examination
- satellite infectious foci (splinter hemorrhages) under fingernails and in conjunctiva due to release of infected material into circulation
- blood culture may be positive for causative organisms
how does one prevent endocarditis?
antibiotic coverage of dental treatment, catheterization in at-risk patients
-bacteremia should be prevented by prophylactic Ab at the time of dental treatment, following current guidelines of AHA
explain what periodontal disease is
chronic inflammation in oral tissues that are in contact with dental plaque
- over years, gingiva detaches from tooth, creating a pocket for microorganism proliferation
- as pocket gets deeper, alveolar bone is destroyed, and mature plaques become calcified
- eventually teeth loosen and are lost
what is “gingivitis” referring to?
early stage periodontal disease
-is reversible if dental hygiene is improved
what is the cause of periodontal disease?
no specific microorganism is responsible, but it’s a mix of anaerobic organisms (mostly G-)
-these organisms are present in small numbers in all people
what is treatment for periodontal disease?
dental hygiene (including regular dental scaling to remove calcified plaque) -periodontal surgery can reduce or eliminate pockets
what is the etiology of diphtheria?
infection of pharyngeal mucous membrane causing necrosis and pseudomembrane with respiratory obstruction
- release of toxin causes systemic muscle paralysis, including myocarditis and death in 10-20% of cases
- mostly a childhood condition
what is the bacteria that causes diphtheria?
Corynebacterium diphtheriae
- G+ club-shaped rods
- metachromatic granules (internal beads)
- stains may be toxigenic (or not); diphtheroids
- inhabit skin and mucus membranes, although carriage may be asymptomatic
what are virulence factors of Corynebacterium diphtheriae?
diptheria toxin encoded by bacteriophage
-causes local and cardiac necrosis
what is a “pseudomembrane”?
necrotic coagulum of bacteria, epithelial cells, fibrin, leukocytes, erythrocytes forming a gray-brown “pseudomembrane” covering the oro-pharynx
how does one diagnose diphtheria?
- swab nose and throat, beneath pseudomembrane
- culture requires tellurite media for C. diphtheria (alert lab)
- confirm toxin production via Ab tests - PCR confirmation of tox gene
*examination of smears is not useful due to existance of non-pathogenic Corynebacteria (diphtheroids)
what is diphtheria treatment?
(equine) antitoxin given as soon as possible
- penicillin or erythromycin helps resolution
- mechanical ventilation as needed
prevention of dihtheria?
- childhood vaccination with toxoid (DTaP)
- boosters after 1 yr, 5 yr
- boosters for adults when traveling to endemic areas (now rare in western world)
does bacteremia occur from rheumatic fever, bacterial endocarditis, periodontal disease, and/or dental extraction?
from bacterial endocarditis and dental extraction
how is diphtheria transmitted?
air-borne droplets
